Aging happens at different speeds from one person to another, but it eventually affects everyone. New research from Stanford Medicine, conducted in mice and human cells, points to a particular failure in the immune system that may help explain why. The researchers found that tissue-resident macrophages, a type of immune cell that lives permanently within organs, become less able with age to dispose of another class of immune cells.
That decline appears to contribute to aging throughout the body. When the scientists blocked a single receptor on these macrophages, multiple organs in mice retained more youthful characteristics. The effects were seen in the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon.
The receptor normally responds to a hormone involved in inflammation and pain in both mice and humans. Disabling the receptor specifically in tissue-resident macrophages also protected mice from several problems associated with chronic inflammation and aging, including frailty, excess fat accumulation and heart trouble. Cognitive decline was substantially reduced as well, according to Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences.
"We've been trying to figure out why we age," Andreasson said. "Now we know at least one big reason for it." The findings are described in a paper published in Science. Andreasson is the senior author, and Jessy Tan, PhD, an instructor in neurology, is the lead author.
The results provide new insight into the important role that chronic, body-wide inflammation plays in aging and its associated health problems. They also point toward a potential drug strategy that could slow age-related deterioration in organs and possibly extend the number of years people remain healthy. How the Immune System Clears Aging Cells Neutrophils are the most abundant white blood cells in the immune system and serve as some of the body's most important first responders.
They are produced in bone marrow and then enter the bloodstream, where they patrol for bacterial, viral, and fungal threats. When neutrophils encounter pathogens, they can release toxic substances and even destroy themselves, spilling long strands of biological material that form web-like traps around invading microbes. These cells do not live for long.
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